ライフサイエンスコーパス: NFAT

1 NFAT activation requires fewer clusters and is more robu

2 NFAT directs the effector arm of the immune response in

3 NFAT DsRed IgE reporter cell binding was significantly i

4 NFAT proteins are important TCR and Ca(2+)-dependent reg

5 NFAT translocates to the nucleus of CFbs on stiffening h

6 NFAT-activated gene expression, triggered in response to

7 NFAT-dependent gene expression is essential for the deve

8 NFAT-dependent transcriptional activity was elevated in

9 NFAT-DsRed IgE reporter cells were sensitized with serum

10 NFAT-DsRed rat basophil leukemia cell attachment and ret

11 We revealed more than 170 NFAT-associated proteins, half of which are involved in

12 We showed that NHA2 is a target of Ca(2+) /NFAT signalling and is transcriptionally induced by meth

13 stin-1 represses NHA2 expression via Ca(2+) /NFAT signalling whereas the dominant negative membrane-a

14 eptor-related orphan receptors on the Ca(2+)-NFAT pathway.

15 n sustaining T cell receptor-mediated Ca(2+)-NFAT signaling and effector functions by repressing sarc

16 Rankl expression, in which JNK and/or Ca(2+)/NFAT pathways were involved and therefore were engaged i

17 ng CRISPR/dead(d)Cas9 targeting of the hHS-8-NFAT site in the human T cell line CEM demonstrate signi

18 ned the ability to flux calcium and activate NFAT-transcription-factor-dependent cytokine production.

19 ucidate the pathway by which G1 can activate NFAT luciferase.

20 contrast, only 3 of 5 were able to activate NFAT (nuclear factor of activated T cells); chimpanzee a

21 utan BILF1 molecules were unable to activate NFAT.

22 t duty cycle and the proportion of activated NFAT in the nucleus.

23 The ensuing Ca(2+) entry then activates NFAT/calcineurin signaling to induce transcriptional pro

24 tion, rendering it ineffective in activating NFAT.

25 Although NFAT is mostly known for its transcription function in t

26 Intriguingly, although NFAT is activated in both DLBCL subtypes, long-term calc

27 Overall, these findings elucidate an NFAT-MAPK signaling paradigm for induction of isletokine

28 and proliferation of cancer stem cells in an NFAT-dependent manner and promotes the development of in

29 uired for NK cell IFN-gamma production in an NFAT-dependent manner, NK cell degranulation/cytotoxicit

30 ility of Zta to attenuate the activity of an NFAT-dependent promoter was shown, which suggests a func

31 Finally, using an NFAT reporter assay, we identified a polyclonal antibody

32 ulin-deficient ESCs or cells treated with an NFAT blocker had enhanced expression of dickkopf WNT-sig

33 downstream activation of NFkappaB, AP-1, and NFAT transcriptional activity.

34 d that the transcription factors Smad2/3 and NFAT-1 are two critical regulators of this process.

35 5222 reduced NFATc3 nuclear accumulation and NFAT-luciferase transcriptional activity in skin microve

36 result in long-lasting calcium activity and NFAT translocation, a measure of full T-cell activation.

37 AKAP79 and NFAT coimmunoprecipitated when coexpressed in heterologo

38 In the human brain, APOE and NFAT are selectively dysregulated in pericytes of APOE4

39 We demonstrate that calcineurin and NFAT factors are constitutively expressed by primary IEC

40 gic or genetic inhibition of calcineurin and NFAT signaling reverses the effects of phenformin on ker

41 , CsA inhibited integrin-LFA-1-dependent and NFAT-independent adhesion of T cells to the intercellula

42 in CLL, where excess programming by EGR and NFAT with reduced EBF and AP-1 programming imbalances th

43 Further, ACK1 promoted calcium flux and NFAT-AP1 promoter activity and decreased the motility of

44 Although c-fos and NFAT often interact to activate gene expression synergis

45 regulatory T (Treg) cells was increased and NFAT-deficient Tregs were fully protective in GvHD.

46 tor engagement for maximal Ca(2+) influx and NFAT activation.

47 vation of the transcription factors JunB and NFAT.

48 ations driving increased MAPK, NF-kappaB and NFAT activity upon T cell receptor stimulation.

49 ines and readouts dependent on NF-kappaB and NFAT.

50 age-gated L-type calcium channels (LTCC) and NFAT translocation to the nucleus following its dephosph

51 eceptor (NPY2R), stimulating PI3K, MAPK, and NFAT activation.

52 ent nuclear translocation of pGFP-NFAT1, and NFAT-dependent but not NFkappaB-dependent gene expressio

53 nt for consensus binding motifs for Nr4a and NFAT transcription factors.

54 t7a induced both canonical Wnt signaling and NFAT and Akt non-canonical signaling.

55 ation in shaping cellular Ca(2+) signals and NFAT activation.

56 ke phenotype involves remodeling of SOCE and NFAT signaling, which together control the expression of

57 or (CTGF), E-cadherin, SRY-box 7 (SOX7), and NFAT (nuclear factor of activated T cells) kinase dual-s

58 transcription factors phosphorylated SP1 and NFAT were master regulators promoting or inhibiting EMT,

59 otifs and had high co-occupancy of STAT5 and NFAT transcription factors (TFs).

60 n by chronic T cell receptor stimulation and NFAT activation.

61 ctors, including CREB, ATF2, C/EBP, USF, and NFAT.

62 phatase whose primary targets in T cells are NFAT transcription factors, and inhibition of calcineuri

63 and interleukin-10, which were identified as NFAT target genes that are particularly important for th

64 (2+)-sensitive transcription factors such as NFAT in ventricular cardiomyocytes.

65 Participants: Participants with benign NFATs ("exposed"; n = 166) and those with no adrenal tum

66 e reciprocal regulatory relationship between NFAT proteins and p53 pathway.

67 Mortality was 11.2% and was similar between NFAT and MACE.

68 No significant associations between NFATs and other outcomes were observed.

69 ary analyses evaluated relationships between NFATs and cortisol physiology.

70 phosphate-mediated signaling and calcineurin-NFAT signaling cascade as important biological process a

71 phy through a cross-talk between calcineurin-NFAT and IKK-NFkappaB pathways.

72 we defined the role of VEGF/Flk1-Calcineurin-NFAT signaling cascade in the transcriptional regulation

73 POE4-mediated CAA and highlights calcineurin-NFAT signaling as a therapeutic target in CAA and Alzhei

74 POE4 carriers, and inhibition of calcineurin-NFAT signaling reduces APOE4-associated CAA pathology in

75 lular senescence, which suggests calcineurin-NFAT signaling as a potential target in preventing PCa.

76 ckdown repressed hypertrophy and calcineurin/NFAT activity.

77 ted cardiac oxidative stress and calcineurin/NFAT signaling in diabetic mice.

78 ted by [Ca(2+)]i chelator BAPTA, calcineurin/NFAT inhibitor VIVIT, and TRPC6 channel knockdown.

79 associated with Ca(2+) handling, calcineurin/NFAT signaling, insulin signaling, cardiac apoptosis and

80 However, calcineurin/NFAT regulation did not contribute to constitutive expre

81 of NFAT-c2, reflecting increased calcineurin/NFAT signaling in myocyte hypertrophy.

82 zed protein CEFIP that modulates calcineurin/NFAT signaling in cardiomyocytes, a finding with possibl

83 RF2) activation independently of calcineurin/NFAT inhibition.

84 it mediates proper regulation of calcineurin/NFAT signaling and COX-2 expression.

85 lets, Ex-4 induced expression of calcineurin/NFAT signaling components as well as target genes for pr

86 omoter activity through PLCgamma/calcineurin/NFAT and MAPK pathways in SaOS-2 and MC3T3-E1 osteoblast

87 ates Sox9 expression through the calcineurin/NFAT signaling pathway during tracheal chondrogenesis.

88 and the ensuing induction of the calcineurin/NFAT, FasL/Fas, and caspase signaling cascades promote n

89 at the suppression of astrocytic calcineurin/NFATs helps to protect synaptic function and plasticity

90 n of the Notch precursor, inhibiting calcium/NFAT and NF-kappaB signaling, and enhancing ERK activati

91 s of the nuclear factor of activated T cell (NFAT) family are essential for antigen-specific T cell a

92 Nuclear factor of activated T cell (NFAT) proteins are activity-dependent transcription fact

93 cineurin/nuclear factor of activated T cell (NFAT) signaling.

94 n of the nuclear factor of activated T cell (NFAT) was also reduced in CaV3.1-deficient T cells.

95 und that nuclear factor of activated T-cell (NFAT) activity is profoundly attenuated if Ca(2+) cleara

96 cineurin/nuclear factor of activated T-cell (NFAT) pathway.

97 urin/nuclear factor of the activated T-cell (NFAT) signaling pathway, and a previously unidentified N

98 ates the nuclear factor of activated T-cell (NFAT) transcription factor but also promotes differentia

99 EB) and nuclear factor of activated T cells (NFAT) and potentiated the transcription of peroxisome pr

100 tion of nuclear factor of activated T cells (NFAT) and the PI3K-AKT kinase-mTOR nutrient-sensing path

101 tion of nuclear factor of activated T cells (NFAT) and Treg proliferation.

102 nsitive nuclear factor of activated T cells (NFAT) c1 transcription factor, as an OC signature gene,

103 of the nuclear factor of activated T cells (NFAT) c3 in lung macrophages, suggesting that inhibitors

104 ineurin/nuclear factor of activated T cells (NFAT) control and is upregulated by calcineurin inhibito

105 nd the nuclear factors of activated T cells (NFAT) family of transcription factors as likely mediator

106 of the nuclear factor of activated T cells (NFAT) family of transcription factors, shows increased e

107 The nuclear factor of activated T cells (NFAT) family proteins are transcription factors that reg

108 factor nuclear factor of activated T cells (NFAT) has a key role in both T cell activation and toler

109 tivates nuclear factor of activated T cells (NFAT) in conduit and medium-sized resistance arteries an

110 ling to nuclear factor of activated T cells (NFAT) luciferase.

111 cause nuclear factor for activated T cells (NFAT) nuclear translocation in VSMCs.

112 ineurin-nuclear factor of activated T cells (NFAT) signaling and APOE in pericyte-like mural cells in

113 induced nuclear factor of activated T cells (NFAT) signaling in subtypes of diffuse large B-cell lymp

114 ediated nuclear factor of activated T cells (NFAT) signaling, long-term potentiation, and responsiven

115 ineurin/nuclear factor of activated T cells (NFAT) signaling.

116 tion of nuclear factor of activated T cells (NFAT) that triggers pathological cardiac and renal fibro

117 ed with nuclear factor of activated T cells (NFAT) transcription factor activity and was sensitive to

118 factor nuclear factor of activated T cells (NFAT) with a similar potency to pMHC in primary murine T

119 tion of nuclear factor of activated T cells (NFAT), a CnAbeta-regulated transcription factor, decreas

120 atenin, nuclear factor of activated T cells (NFAT), and major signaling molecules, resulted in signif

121 factors nuclear factor of activated T cells (NFAT), nuclear factor kappaB (NF-kappaB), and activator

122 os- and nuclear factor of activated T cells (NFAT)-dependent genes.

123 nstream nuclear factor of activated T cells (NFAT)-transcriptional and P300/CBP-associated factor (PC

124 ion via nuclear factor of activated T cells (NFAT).

125 of the nuclear factor of activated T cells (NFAT).

126 F4) and nuclear factor of activated T cells (NFAT).

127 factor nuclear factor of activated T cells (NFAT).

128 by the nuclear factor of activated T-cells (NFAT) depends upon Ca(2+) influx through voltage-gated L

129 ineurin/nuclear factor of activated T-cells (NFAT) pathway and the production of interleukin 8 trigge

130 tion of nuclear factor of activated T-cells (NFAT) transcription factors, and TNFalpha production.

131 in (Cn)-nuclear factor of activated T-cells (NFAT)-mediated hypertrophic signaling, which was reliant

132 ERK) or nuclear factor of activated T-cells (NFAT).

133 tion of nuclear factor of activated T cells (NFATs) in mDA neurons.

134 endent (nuclear factor of activated T cells, NFAT) VAV1 effector pathways.

135 AD through a mechanism involving aberrant CN/NFAT signaling and impaired glutamate transport.

136 Blockade of the astrocytic CN/NFAT pathway in rats using adeno-associated virus (AAV)

137 The blockade of astrocytic CN/NFAT signaling in a common mouse model of AD, using aden

138 However, the impact of astrocytic CN/NFAT signaling on neural function/recovery after acute i

139 Lastly, the CN/NFAT-signaling inhibitor INCA-6 was shown to reduce TNFa

140 s Nox2 and Nox4, indicating that the CnAbeta/NFAT pathway modulates Nox.

141 Many of these elements contain composite NFAT/AP-1 sites, which typically support cooperative bin

142 this study, we show that a highly conserved NFAT binding site within the distal noncoding element hH

143 tively, these findings identify constitutive NFAT signaling as a crucial functional driver of ABC DLB

144 We identified critical NFAT binding motifs in the AQP5 promoter that are involv

145 itive to inhibition of calcineurin-dependent NFAT activation.

146 0 gene was mediated by calcineurin-dependent NFAT signaling in pancreatic beta-cells in response to o

147 mphoid-biased HSCs through calcium-dependent NFAT signaling, providing molecular insights into the ba

148 however, coexpression with PMCA4a depressed NFAT.

149 ry peptide revealed that FOXP3 downregulates NFAT-driven promoter activity of CD40L and IL-17.

150 identify a crucial role for RIPK3-PGAM5-Drp1/NFAT signalling in NKT cell activation, and further sugg

151 n vitro and in vivo, mediated via the DYRK1A-NFAT pathway.

152 signaling, play no role in activating either NFAT protein.

153 h the PMCA4b splice variant further enhanced NFAT activity; however, coexpression with PMCA4a depress

154 cineurin (CN)-dependent transcription factor NFAT (Nuclear Factor of Activated T cells) mediates dele

155 ndent activation of the transcription factor NFAT (Nuclear Factor of Activated T cells) selectively,

156 NOR1) by the initiating transcription factor NFAT (nuclear factor of activated T cells)(10-12).

157 act physically with the transcription factor NFAT (nuclear factor of activated T-cells) that binds to

158 ive complex between the transcription factor NFAT and FOXP3, a lineage specification factor for Tregs

159 we demonstrate that the transcription factor NFAT controls the program of T cell exhaustion.

160 hat the activity of the transcription factor NFAT is chronically elevated in both DLBCL subtypes.

161 m and activation of the transcription factor NFAT.

162 ma2, and its downstream transcription factor NFAT.

163 te the Ca(2+)-dependent transcription factor NFAT.

164 ear localization of the transcription factor NFAT.

165 a model of downstream transcription factor (NFAT) activation, we demonstrate that there is a high co

166 pathways, complexes of transcription factors NFAT and AP-1 promote effector T cell differentiation.

167 Activation induced the transcription factors NFAT and AP-1 which created thousands of new DNase I-hyp

168 ed calcium biosensor Twitch1 and fluorescent NFAT.

169 ogether, these studies show a clear role for NFAT-signaling in TNFalpha-induced retinal leukostasis,

170 ere enriched for consensus binding sites for NFAT and Nr4a family members, indicating that chronic st

171 FOXP3/NFAT interaction is required to repress expression of IL

172 hort synthetic peptide able to inhibit FOXP3/NFAT interaction impaired suppressor activity of convent

173 Inhibition of FOXP3/NFAT interaction upregulated CD40L expression on effecto

174 Specific inhibition of FOXP3/NFAT interaction with this inhibitory peptide revealed t

175 se activity and increased transcription from NFAT or NF-kappaB response element reporters, respective

176 of cytotoxic T lymphocyte effector functions.NFAT nuclear translocation has been shown to be required

177 TIM1-mediated control of Ca(2+) clearance in NFAT induction during T-cell activation.

178 antitumor activity were largely preserved in NFAT-deficient effector T cells.

179 tivation of transcription factors, including NFAT and Egr2/3.

180 ored the specific contribution of individual NFAT factors in donor T cells in animal models of GvHD a

181 tudy was to determine the role of individual NFAT isoforms in TNFalpha-induced retinal leukostasis.

182 transfected with siRNA targeting individual NFAT isoforms were treated with TNFalpha, and qRT-PCR wa

183 We found that LMW-FGF-2 induced NFAT and Ets1 binding to conserved cis-elements in the p

184 uate KCa3.1 as a modulator of Ca(2+)-induced NFAT-dependent osteoclast differentiation in inflammator

185 hat mTOR and CHEK1 kinase activity influence NFAT's transcriptional potency.

186 cific signal transduction pathways involving NFAT or C/EBPbeta transcription factors.

187 Although IL-33 induces AP-1 and NF-kappaB, NFAT signaling has not been described in ILC2s.

188 e inducible transcription factors NF-kappaB, NFAT, and AP-1.

189 c cellular transcription factors (NF-kappaB, NFAT, and STAT5), and that inhibition of Hsp90 greatly r

190 s (</=50 nmol/L) were associated with larger NFAT size and higher prevalence of type 2 diabetes.

191 mentary to this, GRK5 null mice exhibit less NFAT transcriptional activity after transverse aortic co

192 s nuclear factor of activated T lymphocytes (NFAT) and NF-kappaB.

193 IMP761 inhibits TCR-mediated NFAT activation and Ag-induced human T cell proliferatio

194 pression of LZTFL1 enhanced the TCR-mediated NFAT signaling, suggesting that LZTFL1 is an important r

195 unity, Martinez et al. report that monomeric NFAT binding in the absence of a transcriptional partner

196 Transcriptome analysis identifies a MYC-NFAT axis important for osteoclastogenesis.

197 the importance of an I-BET151-inhibited MYC-NFAT axis in osteoclastogenesis, and suggest targeting e

198 ) Jurkat cells displayed defective NFkappaB, NFAT, and MAPK activities owing to attenuated surface ex

199 horylation to stimulate downstream NFkappaB, NFAT, and AP-1 transcriptional activity.

200 In this study, we report a nonredundant NFAT-dependent role for lipid-derived leukotrienes (LTs)

201 activation, acinar cell death, activation of NFAT and NF-kappaB, and inflammatory responses in ex viv

202 found no evidence that DeltaNT activation of NFAT is dependent on Galphaq/11-mediated or beta-arresti

203 (including TGFalpha shedding, activation of NFAT luciferase, and beta-arrestin recruitment) but redu

204 Activation of NFAT requires dephosphorylation by the calcium-dependent

205 ion, and calcineurin-dependent activation of NFAT, the master transcription factor regulating IL-2 ex

206 ardioprotective effect through activation of NFAT/NFkappaB, downregulation of Bnip3, and inhibition o

207 ation of SPPL3 in a screen for activators of NFAT, a transcription factor that controls lymphocyte de

208 Sustained association of NFAT and p300 histone acetyltransferase with the IP-10 g

209 ment-2 site without affecting the binding of NFAT or AP-1 alone to DNA.

210 Finally, our dataset of NFAT-associated proteins provides a good basis to furthe

211 ature to determine the isoform and degree of NFAT activation.

212 nd calcineurin-mediated dephosphorylation of NFAT.

213 rget of rapamycin-1 (mTOR) and expression of NFAT and Myc transcription factors, abrogating the energ

214 LP region with the corresponding fragment of NFAT transcription factor, perfectly matching the previo

215 In vivo inhibition of NFAT may represent a novel therapeutic modality to prese

216 Thus, specific inhibition of NFAT opens an avenue for an advanced therapy of GvHD mai

217 could be mimicked by chemical inhibition of NFAT translocation.

218 Our results suggest that inhibition of NFAT/FOXP3 interaction might improve antitumor immunothe

219 itor the stiffness-dependent localization of NFAT, a downstream target of intracellular calcium signa

220 Critically, measurements of NFAT mobility in neurons employing fluorescence recovery

221 The mechanism of NFAT activation by Ca(2+) has been determined.

222 ntify as yet unknown interaction partners of NFAT, we purified biotin-tagged NFATc1/alphaA, NFATc1/be

223 hannels drastically decreased recruitment of NFAT and histone modifications within key gene loci invo

224 ied by cardiac fibrosis and up-regulation of NFAT-c2, reflecting increased calcineurin/NFAT signaling

225 In leukocytes, Ca(2+) regulation of NFAT-dependent gene expression oftentimes involves the a

226 alcineurin, a calcium-dependent regulator of NFAT, synergistically suppressed HIV reactivation induce

227 icle we demonstrate a major positive role of NFAT family members in Tfh differentiation.

228 COS-iCOSL in T helper cells, and the role of NFAT in regulating the immune response, were affected by

229 Here we investigated the role of NFAT-interacting protein (NIP)-45, an Interleukin (IL)-4

230 nes by facilitating nuclear translocation of NFAT and dephosphorylation of dynamin-related protein 1

231 g complex regulates nuclear translocation of NFAT and its signaling.

232 alcineurin, whereas nuclear translocation of NFAT is associated with increased death from CRC.

233 theta, and impaired nuclear translocation of NFAT, AP-1, and NF-kappaB.

234 alpha, which caused nuclear translocation of NFAT.

235 rease in ICa, T and nuclear translocation of NFAT.

236 und preferentially in the direct vicinity of NFAT-binding motifs and in a distinct orientation to the

237 EGR1, dictates the gene regulatory action of NFATs.

238 ciated with an increase in the activities of NFATs 1 and 4 in the hippocampus at 7 d after injury.

239 were abrogated by calreticulin deficiency or NFAT blockade.

240 second-messenger generation, and JAK/STAT or NFAT transcriptional responses.

241 We experimentally validated the predicted NFAT/Sp1 signaling axis for each phenotype response.

242 Expression of TAK1DeltaN also promoted NFAT (nuclear factor of activated T-cells) transcription

243 Similarly, VEGF promoted NFAT activation and subsequent Adamts-1 induction in aor

244 the AKAP79/150 LZ motif functions to recruit NFAT to the LTCC signaling complex to promote its activa

245 endent control of Ca(2+) clearance regulates NFAT activity during T-cell activation.

246 ts indicate that AS differentially regulates NFAT pathway through PML and p53 and reveal an intricate

247 P expression, suggesting that Wnt7a requires NFAT signaling to exert this function.

248 nchronized VSMC showed 39-fold higher Rgs16 (NFAT (nuclear factor of activated T-cells) target; MAPK

249 Direct evidence showing NFAT activation initiates primary tumor formation in viv

250 esis, reduced TRPC1 expression, and silenced NFAT-transcriptional and PCAF-epigenetic cascades.

251 lated in PDE3B(-/-)mice WAT, including smad, NFAT, NFkB, and MAP kinases.

252 function, is up-regulated in KGM-H via SOCE/NFAT-dependent gene expression.

253 esulted in loss of depolarization-stimulated NFAT signaling in rat hippocampal neurons.

254 teins provides a good basis to further study NFAT's diverse functions and how these are modulated due

255 BI 749327 suppresses NFAT activation in HEK293T cells expressing wild-type or

256 Surprisingly, NFAT activation is independent of B-cell receptor signal

257 transcription function in the immune system, NFAT also has essential functions even in the central ne

258 nts were more prevalent in MACE (15.5%) than NFAT (6.4%).

259 re likely to develop and worsen in MACE than NFAT.

260 nd medium-sized resistance arteries and that NFAT blockade abolishes diabetes-driven aggravation of a

261 sues with NFATc1 activation, indicating that NFAT oncogenic effects depend on cell types and tissue c

262 Our data show that NFAT promotes T cell anergy and exhaustion by binding at

263 omatin immunoprecipitation data suggest that NFAT proteins likely directly participate in regulation

264 Although the NFAT proteins have been extensively investigated in the

265 the astrocyte-specific promoter Gfa2 and the NFAT inhibitory peptide VIVIT reduced signs of glutamate

266 the astrocyte-specific promoter Gfa2 and the NFAT-inhibitory peptide VIVIT prevented the injury-relat

267 creen to identify compounds that disrupt the NFAT:AP-1:DNA complex.

268 lacetamide (Compound 10), which disrupts the NFAT:AP-1 interaction at the composite antigen-receptor

269 voked c-fos activation without impacting the NFAT pathway or Orai1 activity.

270 However, inhibiting the NFAT pathway impaired Wnt7a's ability to inhibit MMP exp

271 Mutagenesis of the NFAT and CRE binding sites, respectively, inhibited the

272 In T cells, members of the NFAT family of transcription factors not only are respon

273 ultimately promote functional binding of the NFAT or C/EBPbeta transcription factors, respectively, t

274 to amino acids within the SP-3 motif of the NFAT regulatory domain.

275 rther, we show small molecules targeting the NFAT pathway alter nuclear translocation of PER and CRY

276 h bound to type 1 IFN promoters and that the NFAT binding site in IFN promoters was required for IRF7

277 s on specific pathways to correctly tune the NFAT, NF-kappaB, and AP-1 activation cascades.

278 P response element (CRE) contiguous with the NFAT binding site in the FGF-23 promoter.

279 Treatment of diabetic mice with the NFAT blocker A-285222 reduced NFATc3 nuclear accumulatio

280 led Tfr and Tfh cell differentiation through NFAT-mediated IRF4, BATF, and Bcl-6 transcription-factor

281 xpression of Zta is itself regulated through NFAT activity, suggesting that Zta may contribute to a f

282 ai1 was able to couple local Ca(2+) entry to NFAT activation, identifying the N-terminal domain of Or

283 new insights into how LTCCs and signaling to NFAT are regulated by this LZ interaction.

284 icited increased downstream signaling toward NFAT activation, and inhibition of this pathway resulted

285 ecause Tregs remain capable of translocating NFAT even in the presence of high CNI levels.

286 ypothesis that nonfunctional adrenal tumors (NFATs) increase risk for cardiometabolic outcomes compar

287 mostly benign nonfunctioning adrenal tumors (NFATs) or adenomas causing mild autonomous cortisol exce

288 aling pathway, and a previously unidentified NFAT binding site is identified within the mouse Sox9 pr

289 During follow-up, NFAT and MACE do not show clinically relevant changes in

290 decreases Nox2 and Nox4 expression, whereas NFAT overexpression increases Nox2 and Nox4, indicating

291 In this study, we test whether NFAT plays a role in the development of endothelial dysf

292 NIPBL-bound enhancers were associated with NFAT, PU.1, and CEBP cis elements, whereas NIPBL-bound p

293 udies suggest that GRK5 acts in concert with NFAT to increase hypertrophic gene transcription in the

294 r evidence for an AKAP79 LZ interaction with NFAT.

295 Only 4.3% of patients with NFAT developed MACE, and preexisting MACE was unlikely t

296 dies reported outcomes of 4121 patients with NFAT or MACE, 61.5% of whom were women; the mean age was

297 unlikely to develop (<0.1%) in patients with NFAT or MACE.

298 lls and their responses correlated well with NFAT translocation to the nucleus, validating the biolog

299 Conclusion: Participants with NFATs had a significantly higher risk for diabetes than

300 Results: Participants with NFATs had significantly higher risk for incident composi